Lazybones, Sorry my interpretation of the definitions varies in several places. Really this should have a new thread since it isn't to do with exercise (so apologies to the original poster)
The idea of the classification used since 1999 is that diabetes is the result of several distinctly different disease processes .
All the quotes are from Definition, Diagnosis and Classification of Diabetes Mellitus and its Complications WHO 1999
In theory, everyone with diabetes goes through a period of prediabetes, even those with fast onset T1 . It is not the treatment but the underlying disease process which separates one type from another. .
People don't change from one type of diabetes to another (unless misdiagnosed)
The old terms IDDM and NIDDM were abandoned because they could indeed confuse.
It is recommended that the terms "insulin-dependent diabetes mellitus" and "non-insulin-dependent diabetes mellitus" and their acronyms "IDDM" and "NIDDM" no longer be used. These terms have been confusing and frequently resulted in patients being classified based on treatment rather than on pathogenesis.
T1
includes "
those cases attributable to an autoimmune process, as well as those with beta-cell destruction and who are prone to ketoacidosis for which neither an aetiology nor a pathogenesis is known (idiopathic)."
T1a autoimmune includes the slowly developing form
LADA
The slowly progressive form generally occurs in adults and is sometimes referred to as latent autoimmune diabetes in adults (LADA). Some patients, particularly children and adolescents, may present with ketoacidosis as the first manifestation of the disease (26). Others have modest fasting hyperglycaemia that can rapidly change to severe hyperglycaemia and/or ketoacidosis in the presence of infection or other stress. Still others, particularly adults, may retain residual beta-cell function, sufficient to prevent ketoacidosis, for many years (27). Individuals with this form of Type 1 diabetes often become dependent on insulin for survival eventually and are at risk for ketoacidosis (28). At this stage of the disease, there is little or no insulin secretion as manifested by low or undetectable levels of plasma C-peptide (29).
Markers of immune destruction, including islet cell autoantibodies, and/or autoantibodies to insulin, and autoantibodies to glutamic acid decarboxylase (GAD) are present in 85-90 % of individuals with Type 1 diabetes mellitus when fasting diabetic hyperglycaemia is initially detected
LADA is probably more well known today (not by some GPs though) It was however defined in the 1999 document quoted above .
People with LADA will become insulin dependent because the autoimmune process destroys the beta cells not because they become more insulin resistant. Many people with LADA are very insulin sensitive.
T1b is :idiopathic(unknown causes) though the example given in the document. A type of diabetes , sometimes called 'Flatbush' where insulin dependency tends to come and go is more often known today as ketosis prone T2. This type only gets the occasional mention in the literature.
Other Specific Types
There are indeed a large number of types of diabetes mellitus that have well known disease cause/process. These are listed in 8 subsets These are a bit in limbo as to name, they are either just called other types of diabetes or occasionally T3 a- h
Amongst them are types of diabetes caused by genetic mutations, those caused by other diseases, those caused by damage or loss of the pancreas.(this last is quite often referred to as 3C)
The misnamed
MODY is not a form of T2. It is listed in this section. It is caused by one of several genetic mutation (we now know of 11, some very rare) It is categorised as a diabetes caused by a genetic defect in insulin secretion. We have recently had people on the forum with
MIDD, (maternally inherited diabetes and deafness this is caused by a genetic mutation in mitochondrial DNA)
whole list here:
Gestational has it's own category.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3006051/table/T1/
T2
I've left T2 until last since it's the hardest to describe. (and this is far to long)
T2 contains a mixture of
all those who haven't evidence of an autoimmune attack and who don't have one of the 'other' defined varieties. The committee actually suggested that as different causes were found some would be removed from the T2 section . They mentioned for example
'a lean phenotype of Type 2 diabetes mellitus in adults found in the Indian sub-continent may be very distinct from the more characteristic form of Type 2 found in Caucasians' but said they didn't have enough information to categorise it separately
T2 includes by far the greatest number of people.
People with it have a combination of relative insulin deficiency and insulin resistance. This varies from person to person and one or other may predominate. ie they may not make enough insulin to counter their own degree of insulin resistance. Often (sorry the document says this) 'people with this form of diabetes are obese, and obesity itself causes or aggravates insulin resistance. '
Some may eventually need insulin. However they do not become T1. and in many cases do not actually require insulin to survive. (in the short term that is)
The first link is to a copy of the committee recommendations, the WHO own link isn't working.
The second is to the easier to read version. This is the 2011 ADA version which is in most places identical but has slight changes to include more recent findings eg, specific gene associations in T1 )
http://www.staff.ncl.ac.uk/philip.home/who_dmc.htm
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3006051/
- this is the transporter that enables glucose to be transported directly into working muscle cells without the need for insulin. When exercising the GLUT4 become mobilised and are charged ready to help transport glucose into hungry muscle cells. This is what improves insulin sensitivity. The effects (as observed with the woman during pregnancy) last longer if exercise has been high intensity.
- another thread is a great idea. 